This unit addresses II. Heart Rate Variability (2 hours).
Professionals
completing this module will be able to discuss:
A. The meaning of HRV
B. The sources of HRV
C. Factors that influence HRV
D. Correlates of low and normal HRV
E. The benefits of increased HRV
This unit covers The Meaning of HRV, The Sources of HRV, Factors that Influence HRV, Correlates of Low and Normal HRV, The Benefits of HRV, and Heart-Brain Interactions.
Please click on the podcast icon below to hear a full-length lecture.
Elevated HR Is Associated with Dementia and Cognitive Decline
Imahori et al. (2021) conducted a cohort study of 2147 adults ≥ 60 who were free of dementia when they entered the study. Resting heart rates (RHR) ≥80 (compared with 60-69 bpm) were associated with a greater risk of dementia and more rapid cognitive decline, independent of cardiovascular disease (CV).
We measure the time intervals between successive heartbeats in milliseconds. Graphic adapted from Dr. Richard Gevirtz.
Faster HRs reduce the time between successive beats and the opportunity for interbeat intervals (IBIs) to vary. Faster HRs lower HRV. Resting HRs that exceed 90 bpm are associated with an elevated risk of mortality (Zhang, Shen, & Qi, 2016).
The next three scatterplots show an inverse relationship between HR and three widely used HRV metrics: RMSSD, SDNN, and low-frequency power.
When the time intervals between heartbeats significantly change
across successive breathing cycles, this shows that the cardiovascular center can effectively modulate vagal tone.
The record below shows healthy variability. The time intervals between successive heartbeats differ.
In contrast, this record shows no variability since the IBIs are identical. This display could represent a heart driven by a pacemaker or a heart that needs one.
"The complexity of a healthy heart rhythm is critical to the maintenance of homeostasis because it provides the flexibility to cope with an uncertain and changing environment...HRV metrics are important because they are associated with regulatory capacity, health, and performance and can predict morbidity and mortality" (Shaffer, Meehan, & Zerr, 2020).
"... HRV is associated with executive function, regulatory capacity, and health... Cardiac vagal control indexes how efficiently we mobilize and utilize limited self-regulatory resources during resting, reactivity, and recovery conditions" (Shaffer, Meehan, & Zerr, 2020).
The vagal tone modulation helps to maintain the dynamic autonomic balance critical to
cardiovascular health. Autonomic imbalance due to deficient vagal inhibition is implicated in increased morbidity
and all-cause mortality (Thayer, Yamamoto, & Brosschot, 2010).
HRV appears to index autonomic functioning, BP, neurocardiac functioning, digestion, oxygen and carbon dioxide exchange, vascular tone (diameter of resistance vessels), and possibly facial muscle regulation (Gevirtz et al., 2016). HRV reflects the vagal contribution to executive functions, affective control, and social self-regulation (Byrd et al., 2015; Laborde et al., 2017; Mather & Thayer, 2018).
Influential HRV Theories
The Vagal Tank Theory frames cardiac vagal control as a dynamic resource for self-regulation and stress resilience, while the Autonomic Space Theory highlights the independent and flexible interplay of sympathetic and parasympathetic activity. Together, they provide a comprehensive framework for understanding HRV as a marker of physiological adaptability, emotional regulation, and cognitive flexibility, informing targeted interventions in health and performance.
Vagal Tank Theory
Vagal Tank Theory conceptualizes cardiac vagal control as a dynamic resource for self-regulation, which can be depleted or replenished. It consists of three Rs: (1) Resting vmHRV, reflecting baseline self-regulation capacity, (2) Reactivity, the vagal withdrawal response to stressors, and (3) Recovery, the ability to restore autonomic balance post-stressor. A higher vagal tank is associated with better stress resilience, emotional regulation, and health outcomes.
Autonomic Space Theory
Autonomic Space Theory (Berntson et al., 1994) challenges the simplistic reciprocal model of autonomic control by proposing three modes: (1) Reciprocal Activation (one branch active, the other suppressed), (2) Coactivation (both sympathetic and parasympathetic systems active), and (3) Coinhibition (both suppressed). This framework highlights the independent and complex nature of autonomic regulation in physiological and emotional processes.
Vagally-Mediated HRV (vmHRV)
Vagally-mediated heart rate variability (vmHRV) has emerged as a critical biomarker for self-regulation and health, offering insights into psychological and physiological adaptation. As a noninvasive and cost-effective tool, vmHRV serves as an actionable measure in various domains, including physical and mental health, social interactions, stress regulation, and performance optimization (Laborde et al., 2023).
The sympathetic nervous system is another source of HRV. Sympathetically-mediated HRV (smHRV) refers to HRV components influenced by the sympathetic nervous system, typically assessed through measures such as low-frequency (LF) power in HRV analysis. However, the interpretation of LF power as a direct marker of sympathetic activity remains debated.
This section draws heavily on Laborde and colleagues' (2023) "Leveraging Vagally Mediated Heart Rate Variability as an Actionable, Noninvasive Biomarker for self-Regulation: Assessment, Intervention, and Evaluation."
vmHRV and Self-Regulation
Heart rate variability, particularly its vagally mediated component, reflects the dynamic interplay between the autonomic nervous system and cognitive-emotional regulation. The neurovisceral integration model (Thayer et al., 2009) posits that vmHRV is linked to self-regulation processes via prefrontal cortical control over the vagus nerve, facilitating adaptive responses to environmental demands. The vagal tank theory (Laborde et al., 2018) extends this perspective by emphasizing vmHRV in three contexts: resting levels, reactivity to stressors, and recovery post-stressor exposure. Higher vmHRV is associated with better cognitive flexibility, emotion regulation, and adaptive physiological responses (Shaffer et al., 2014).
Health Implications of vmHRV
Cardiovascular Health
The autonomic nervous system (ANS) plays a critical role in maintaining physiological stability, and vagally mediated heart rate variability (vmHRV) is an essential biomarker of its function. Higher vmHRV is indicative of robust parasympathetic activity, which is associated with greater adaptability to environmental and internal stressors, whereas lower vmHRV is linked to autonomic dysregulation and increased health risks. One of the most well-established associations of vmHRV is with cardiovascular health.
Numerous studies have demonstrated that lower vmHRV is a predictor of cardiovascular disease (Hillebrand et al., 2013), including hypertension, atherosclerosis, and heart failure. Individuals with higher vmHRV tend to exhibit greater cardiovascular efficiency, characterized by better baroreceptor sensitivity, improved endothelial function, and enhanced myocardial perfusion. In contrast, individuals with diminished vmHRV often show increased arterial stiffness, reduced heart rate recovery following exertion, and an overall heightened risk for adverse cardiac events, including myocardial infarction and stroke.
Metabolic Regulation
Beyond cardiovascular health, vmHRV has significant implications for metabolic regulation. Research has consistently linked low vmHRV to metabolic disorders such as diabetes mellitus (Benichou et al., 2018), insulin resistance, and obesity. The autonomic imbalance observed in individuals with lower vmHRV contributes to dysregulated glucose metabolism, increased systemic inflammation, and greater susceptibility to metabolic syndrome. High vmHRV, on the other hand, is associated with better glycemic control and improved pancreatic beta-cell function. The modulation of insulin sensitivity via vagal pathways suggests that vmHRV-enhancing interventions, such as slow-paced breathing and vagus nerve stimulation, could serve as valuable therapeutic strategies for individuals with metabolic disorders.
Immune Function
Another critical aspect of vmHRV’s health implications is its connection to immune function. The cholinergic anti-inflammatory pathway, which is mediated by vagal activity, plays a pivotal role in regulating inflammatory responses (Williams et al., 2019). Lower vmHRV is associated with increased levels of pro-inflammatory cytokines such as interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-a), and C-reactive protein (CRP), which are implicated in the pathogenesis of numerous chronic diseases, including autoimmune conditions, neurodegenerative diseases, and cancer. Conversely, higher vmHRV is correlated with an anti-inflammatory state, which facilitates faster recovery from infections and injuries while mitigating chronic inflammation-related pathologies. This has led to growing interest in using vmHRV as a biomarker for immune resilience, particularly in conditions such as rheumatoid arthritis, lupus, and inflammatory bowel disease.
Stress and Sleep Regulation
The relationship between vmHRV and stress-related health outcomes is particularly compelling. Chronic stress and prolonged exposure to environmental or psychological stressors contribute to dysregulation of the hypothalamic-pituitary-adrenal (HPA) axis and sustained autonomic imbalance. Individuals with lower vmHRV exhibit heightened sympathetic activity and reduced parasympathetic regulation, leading to persistently elevated cortisol levels, increased oxidative stress, and greater allostatic load. This autonomic dysfunction is linked to a range of stress-related conditions, including irritable bowel syndrome, chronic fatigue syndrome, and fibromyalgia. In contrast, individuals with higher vmHRV demonstrate more efficient stress recovery mechanisms, allowing for better emotional and physiological resilience to stressors. The ability of vmHRV to reflect these underlying mechanisms has made it a valuable tool for understanding stress-related illnesses and developing targeted interventions.
The significance of vmHRV in sleep regulation further highlights its broad health implications. Sleep disturbances, including insomnia, sleep apnea, and restless leg syndrome, have been associated with reduced vmHRV, indicating impaired autonomic balance during sleep (Chouchou & Desseilles, 2014). Poor sleep quality contributes to a cascade of negative health outcomes, including impaired cognitive function, weakened immune defense, and increased risk of metabolic and cardiovascular diseases. Individuals with higher vmHRV tend to experience more stable sleep patterns, enhanced slow-wave sleep, and improved nocturnal autonomic regulation, which collectively support overall well-being and cognitive performance.
Clinical and Psychological Relevance
Mental Health Disorders
In clinical psychology and psychiatry, vmHRV is increasingly recognized as a transdiagnostic biomarker of mental health and emotional regulation. Individuals with low vmHRV consistently exhibit greater vulnerability to psychiatric disorders, including anxiety disorders, major depressive disorder (MDD), posttraumatic stress disorder (PTSD), and bipolar disorder (Beauchaine & Thayer, 2015). Reduced vmHRV in these populations reflects diminished vagal regulation of emotional responses, heightened sympathetic arousal, and impaired top-down control from prefrontal cortical regions. This dysregulation contributes to increased emotional reactivity, maladaptive coping mechanisms, and difficulty modulating physiological responses to stressors.
For anxiety disorders, lower vmHRV is associated with excessive autonomic arousal, persistent worry, and hypervigilance (Wang et al., 2023). Individuals with generalized anxiety disorder (GAD) often show reduced parasympathetic tone, leading to increased heart rate, respiratory irregularities, and prolonged physiological recovery from stressors. Similarly, individuals with PTSD exhibit pronounced autonomic dysregulation, with lower vmHRV reflecting impaired fear extinction and heightened amygdala reactivity to trauma-related cues. Targeted interventions such as heart rate variability biofeedback and vagal nerve stimulation have shown promise in improving autonomic regulation and reducing symptoms of hyperarousal in these populations.
HRV is produced by interacting regulatory mechanisms that operate on
different time scales (Moss, 2004). Circadian rhythms, core body temperature, and metabolism contribute to 24-hour
HRV recordings, representing the "gold standard" for clinical HRV assessment. The parasympathetic,
cardiovascular, and respiratory systems produce short-term (e.g., ~ 5-minute) HRV measurements.
Respiratory sinus arrhythmia, the baroreceptor reflex, and the vascular tone rhythm are the most important sources of HRV (Hayano & Yuda, 2019; Vaschillo et al., 2002).
Vaschillo’s two closed-loop model explains how HRV biofeedback procedures like slow-paced breathing (SPB) and slow-paced contraction (SPC) can increase HRV. Vaschillo et al. (2002) described the heart rate (HR) and vascular tone (VT) baroreflexes as closed loops and proposed that stimulating one closed loop activates its counterpart. Graphic adapted from Vaschillo et al. (2002).
Each baroreflex is a potential target for HRV biofeedback training. SPB and SPC at ~ 6 bpm/cpm can stimulate the HR baroreflex, separately or synergistically. SPC at ~ 1 cpm can activate the VT baroreflex.
Note. Bottom left: the lung and muscle icons indicate that SPB and SPC, alone or together, can stimulate the HR baroreflex ~ 6 bpm/cpm. Bottom right: the muscle icon signals that SPC can activate the VT baroreflex ~ 2 cpm.
Respiratory sinus arrhythmia (RSA), HR speeding and slowing across each breathing cycle, is the primary and entirely parasympathetic source of HRV (Gevirtz, 2020).
In the graphic adapted from Elite Academy below, the blue waveform represents the breathing cycle, and the red signals are heartbeats. Note that the heartbeats are spaced more closely (HR speeds) during inhalation and farther apart (HR slows) during exhalation.
Inhalation disengages the vagal brake, speeding HR. This is purely parasympathetic. Graphics inspired by Dr. Gevirtz. Artist: Dani S @ unclebelang on Fiverr.
Exhalation reapplies the vagal brake, slowing HR.
Inhalation speeds the heart, and about 5 seconds later, BP falls. During exhalation, the heart slows, and about 5 seconds later, BP increases. Graphic adapted from Evgeny Vaschillo.
Note. The bottom line represents respiration. A rising black bar is inhalation, and a falling black bar means exhalation. The following lines represent HR and BP. This diagram allows us to see the changes in HR and BP produced by breathing.
Slow-Paced Breathing and Slow-Paced Muscle Contraction Stimulate Vaschillo's Two Closed Loops
Respiratory sinus arrhythmia, the baroreceptor reflex, and the vascular tone rhythm are the most important sources of short-term (~ 5-minute) HRV. These processes are exclusively parasympathetic (Hayano & Yuda, 2019; Vaschillo et al., 2002).
We can stimulate the HR and VT baroreflexes using slow-paced breathing and slow-paced contraction protocols.
Targeting the Heart Rate Baroreceptor Reflex
Slow-paced breathing (~ 6 bpm) and slow-paced contraction (~ 6 cpm) can increase HR oscillations and HRV, separately or synergistically.
Slow-Paced Breathing
Let's start with SPB. Respiration can produce blood pressure oscillations via changes in thoracic pressure (Pinsky, 2018) that can stimulate the closed loops.
Before HRVB, respiration and the baroreflex are usually out of phase, resulting in weak resonance effects (i.e., HR changes).
Graphics adapted from Elite HRV.
HRV biofeedback training slows breathing to the baroreflex’s rhythm, which aligns these processes and significantly increases resonance effects.
Slowing breathing to rates between 4.5-6.5 bpm for adults and 6.5-9.5 bpm for children increases RSA (Lehrer & Gevirtz, 2014). Increased RSA immediately “exercises” the baroreflex without changing vagal tone or tightening BP regulation. Those changes require weeks to months of practice. HRV biofeedback can immediately increase RSA 4-10 times compared to a resting baseline (Lehrer et al., 2020b; Vaschillo et al., 2002). Graphic adapted from Gevirtz et al. (2016).
Note. The red waveform shows HR oscillations while resting without breathing instructions or feedback. The blue waveform shows HR oscillations with HRV biofeedback and breathing from 4.5-6.5 bpm.
Slow-paced contraction (wrists-core-ankles with legs crossed) at ~ 6 and 2 cpm may stimulate blood pressure, HR, and VT control systems without slowing respiration (Vaschillo et al., 2011). This video does not include an audio track.
Like slow-paced breathing, slow-paced contraction amplifies heart rate oscillations. Slow-paced contraction stimulates the HR baroreflex at ~ 6 cpm and the VT baroreflex at ~ 2 cpm to immediately increase HRV. Weeks to months of practice are required to increase vagal tone.
Maximum-Minimum HR for each breath indexes RSA. The peak frequency is the HRV frequency with the greatest power. In the screen captures below, SPC stimulated the baroreceptor reflex at the intended frequency (0.2 Hz for 12 cpm and 0.1 Hz for 6 cpm).
Shaffer, Moss, and Meehan (2022) reported that slow-paced contraction at 1 and 6 cpm increased five time-domain metrics (HR Max – HR Min, RMSSD, SDNN, TI, and TINN), one frequency-domain metric (LF power), and three non-linear metrics (D2, SD1, SD2) to a greater degree than slow-paced contraction at 12 cpm. There were no differences between the 1 and 6 cpm conditions.
Meehan and Shaffer (2023) compared 6-cpm wrist-ankle slow-paced contraction with 6-cpm wrist-core-ankle slow-paced contraction. Both conditions produced greater HR, HR Max-HR Min, and LF power than the control condition. The wrist-core-ankle method yielded greater HR and HR Max-HR Min than wrist-ankle slow-paced contraction.
Note. Descriptive statistics represent the results of untransformed, raw data. Error bars represent the 95% confidence interval around the mean.
Note. Descriptive statistics represent the results of untransformed, raw data. Error bars represent the 95% confidence interval around the mean.
Factors That Influence HRV
Critical factors influencing HRV include age, circadian effects, HR, resonance, respiration rate, and depth.
Almedia-Santos et al. (2016) obtained 24-hour ECG recordings of 1743 subjects 40-100 years of age. They found a linear decline in the SDNN, the standard deviation of the average NN intervals for each 5-minute segment (SDANN), and the standard deviation of NN intervals (SDNN index). However, they found a U-shaped pattern for the RMSSD and pNN50 with aging, decreasing from 40-60 and then increasing after age 70. The age groups were 1 (40–49 years), 2 (50–59 years), 3 (60–69 years), 4 (70–79 years), and 5 ( = 80 years).
We discussed cycle length dependence earlier. Faster HRs decrease the opportunity for IBIs to vary in length, whereas slower HRs increase the chance of beat-to-beat differences.
Resonance
Resonance is an amplification process that relies on simple physics (Lehrer, 2020). An external force causes a closed-loop (negative feedback) system to oscillate with greater amplitude at its inherent resonance frequency (RF). Here are four examples.
Finally, overloading a wine glass with sound at its RF can cause it to shatter because it cannot withstand the vibrational energy. Graphic courtesy of MARTY33 of YouTube.
The baroreflex system exhibits resonance since it is a feedback system with a fixed delay. Inertia due to blood volume in the vascular tree accounts for most of this delay.
You can observe the effect of a breathing rate on RSA during paced breathing and select the rate that produces the largest HR oscillations.
Adult breathing from 4.5-6.5 bpm shifts the ECG peak frequency from the high-frequency band (~0.20 Hz) to the cardiovascular system’s RF (~0.10 Hz). This more than doubles the energy in the low-frequency band of the ECG (0.04-0.15 Hz).
We train clients to increase low-frequency power and RSA so that high-frequency power and time-domain measures like the RMSSD will increase during baselines when breathing at typical rates (Lehrer, 2020).
Breathing Rate and Depth
RSA increases with greater respiratory depth (Hirsch & Bishop, 1981) and lowers respiration rate (Brown et al., 1993). A 10-s breathing cycle corresponds to a 6-bpm respiration rate in the graphic below. This rate falls within the 4.5-6.5 adult RF range.
The graphic below was adapted from Grossman and Kollai (1993). RSA, shown as a change in heart rate from inhalation to exhalation, increases as the respiration rate approaches 6 bpm.
Correlates of Low and Normal HRV
Heart Rate Variability Is Desirable, While Blood Pressure Variability Is Dangerous
Heart rate variability biofeedback is extensively used to treat various disorders (e.g., asthma and depression) and enhance performance in various contexts (e.g., sports; Gevirtz, 2013; Lehrer et al., 2020a; Tan et al., 2016).
Lehrer et al. (2020) observed that “…HRVB has the largest effect sizes on anxiety, depression, anger, and athletic/artistic performance and the smallest effect sizes on PTSD, sleep, and quality of life” (p. 109).
Although the final targets of these applications may differ, HRVB increases vagal tone (Vaschillo et al., 2006) and stimulates the negative feedback loops responsible for homeostasis (Lehrer & Eddy, 2013).
Whereas HRV is desirable, BP variability can endanger health. We require BP stability under constant workloads (Gevirtz, 2020). Graphic adapted from Dr. Gevirtz by Minaanandag on fiverr.com.
Reduced HRV Is Associated with Disease and Loss of Adaptability
In the early 1960s, researchers found that changes in HRV preceded fetal distress (Hon & Lee, 1963).
Reduced HRV is associated with vulnerability to physical and psychological stressors and disease (Lehrer, 2007). Prospective studies have shown that decreased HRV is the strongest independent predictor of coronary atherosclerosis progression (McCraty & Shaffer, 2015).
Low HRV is a marker for cardiovascular disorders, including hypertension, especially with left ventricular
hypertrophy; ventricular arrhythmia; chronic heart failure; and ischemic heart disease (Bigger et al., 1995;
Casolo et al., 1989; Maver, Strucl, & Accetto, 2004; Nolan et al., 1992; Roach et al., 2004). Low HRV predicts
sudden cardiac death, especially due to arrhythmia following myocardial infarction and post-heart attack survival
(Bigger et al., 1993; Bigger et al., 1992; Kleiger et al., 1987).
Depression in myocardial infarction (MI) patients increases mortality. Depressed patients are twice as likely as non-depressed individuals to have lower HRV (16% vs. 7%). Lower HRV is a strong independent predictor of post-MI death (Craney et al., 2001). HRVB might reduce anxiety and depression, which are associated with low vagal activity, because it increases vagal tone. From Friedman’s (2007) perspective, the problem is not “a sticky accelerator.” HRVB may fix “bad brakes” (p. 186).
Reduced HRV may predict disease and mortality because it indexes reduced regulatory capacity, which is the ability to adaptively surmount challenges like exercise and stressors. Patient age may be an essential link between reduced HRV and regulatory capacity since HRV and nervous system function decline with age (Shaffer, McCraty, & Zerr, 2014).
Reduced HRV is also seen in disorders with autonomic dysregulation, including anxiety and depressive disorders, asthma, and vulnerability to sudden infant death (Agelink et al., 2002; Carney et al., 2001; Cohen &
Benjamin, 2006; Giardino, Chan, & Borson, 2004; Kazuma, Otsuka, Matsuoka, & Murata, 1997). Lehrer (2007) believes that HRV indexes adaptability and marshals evidence that increased RSA represents more
efficient regulation of BP, HR, and gas exchange by synergistic control systems.
The Benefits of Increased HRV
The core benefits of increased HRV are enhanced RSA, low-frequency band power, carbon dioxide and oxygen regulation, baroreflex gain and blood pressure (BP) regulation, modulation of immunity, and remodeling damaged hearts.
RSA
When clients breathe at their resonance frequency, HR and respiration are in perfect phase (0o); their peaks and valleys coincide. This frequency in adults varies from 4.5 to 6.5 breaths per minute (Gevirtz, Lehrer, & Schwartz, 2016). When clients breathe at this rate, they "exercise" the baroreflex.
Resonance frequency (RF) breathing amplifies the swings in HR produced by the baroreflex, increasing baroreflex gain and RSA. RF breathing also modulates blood pressure changes since HR and BP oscillations are 180o out of phase (DeBoer, Karemaker, & Strackee, 1987; Vaschillo et al., 2002).
Low-frequency Band Power
RF breathing shifts the peak frequency from the high-frequency band (~0.20 Hz) to the cardiovascular system’s RF (~0.10 Hz). RF breathing more than doubles the energy in the low-frequency band of the ECG (0.04-0.15 Hz).
This corresponds to the Institute of HeartMath's concept of coherence, in which a client produces a "narrow,
high-amplitude, easily visualized peak" from 0.09-0.14 Hz (Ginsberg, Berry, & Powell, 2010, p. 54; McCraty
et al., 2009).
Increased baroreflex gain means that the
cardiovascular system produces large-scale HR increases and decreases when a client inhales and exhales. This, in
turn, translates into greater HRV.
Modulation of Immunity
Like vagal nerve stimulation (VNS), resonance frequency breathing may also influence the parasympathetic cholinergic cytokine control system that modulates immunity through interleukins and interferons (Gevirtz, 2013; Tracey, 2007).
The sensory vagus detects inflammation/infection via tissue necrosis factor (TNF) and interleukin-1 (IL-1). The motor vagus signals descending neurons to release norepinephrine to spleen T cells, prompting these cells to release acetylcholine to macrophages to dampen inflammation (Schwartz, 2015).
Lehrer et al. (2010) demonstrated that subjects trained to breathe at their RF minimized the
reduction of HRV, headache, and eye photosensitivity following an injection of lipopolysaccharide (LPS), an inflammatory cytokine.
Remodeling Failing Hearts
Moravec and McKee (2013) reported preliminary evidence that HRV biofeedback may act like a left ventricular assist
device (LVAD) to help remodel failing hearts.
HRV biofeedback for heart failure patients represents a
paradigm shift. Instead of only targeting sympathetic activation, HRV biofeedback teaches patients to restore
autonomic balance by decreasing SNS arousal while increasing PNS activity.
Just as we only expect athletes to lift weights during workouts, we don’t expect clients to walk around breathing at 6 bpm constantly. They do not have to continuously breathe at your RF to benefit from improved homeostatic regulation, regulatory capacity, and executive function. Continuous RF breathing would jeopardize homeostasis since breathing rate and volume should adjust to changing daily physical workloads.
0.1 Hz biofeedback: training to concentrate ECG power around 0.1 Hz in the low
frequency (LF) band by teaching patients to breathe diaphragmatically at their RF around 6 breaths per
minute and to experience positive emotional tone to maximize heart rate variability.
abdominal excursion: the degree of outward and inward stomach movement across the breathing cycle.
autonomic space theory: Berntson and colleagues challenged the reciprocal model of autonomic control, proposing that sympathetic and parasympathetic systems can function independently. It identifies three modes: reciprocal activation, coactivation, and coinhibition, highlighting the complex interplay of autonomic regulation in stress, cognition, and physiological adaptability.
baroreceptors: BP sensors located in the aortic arch and internal
carotid arteries.
baroreceptor gain: increased baroreceptor sensitivity to BP changes.
baroreceptor reflex (baroreflex):
a mechanism that provides negative feedback control of BP. Elevated BP activates the baroreflex to
lower BP and low BP suppresses the baroreflex to raise BP.
chemoreceptor: sensors that detect oxygen and carbon dioxide in the blood to
regulate gas concentration.
chaos: unpredictability due to nonlinear dynamics.
cycle length dependence: the phenomenon where faster HRs reduce the time between successive beats and the opportunity for the interbeat intervals (IBIs) to vary, resulting in lower HRV.
D2: correlation dimension estimates the minimum number of variables required to construct a system dynamics model.
epinephrine (E): an adrenal medullary hormone that increases muscle blood flow, converts stored nutrients into glucose for use by skeletal muscles, and initiates cardiac muscle contraction when it binds to β1 receptors.
fractals: infinitely complex geometric patterns that are self-similar across different scales.
frequency-domain measures of HRV: the absolute or relative power of
the HRV signal within four frequency bands.
heart rate baroreflex: the closed-loop encompassing the cardiovascular control center, heart rate control system, and blood pressure control system.
heart rate variability (HRV): the beat-to-beat changes in HR involving
changes in the RR intervals between consecutive heartbeats.
high-frequency (HF) band: an ECG frequency range from 0.15-0.40 Hz that represents the inhibition and activation of the vagus nerve by breathing (RSA).
homeostasis: a state of dynamic constancy achieved by stabilizing conditions about a setpoint, whose value may change over time.
HR Max – HR Min: an HRV index that calculates the average difference between the highest and lowest HRs during each respiratory cycle.
HRV frequency-domain measurements: metrics that quantify absolute or relative power distribution into four frequency bands, revealing the sources of HRV.
HRV nonlinear measurements: metrics that quantify the unpredictability of a time series, resulting from the complexity of the mechanisms that regulate the measured variable.
HRV time-domain measurements: metrics that quantify the total amount of HRV.
interbeat interval (IBI): the time interval between the peaks of successive R-spikes
(initial upward deflections in the QRS complex). This is also called the NN (normal-to-normal) interval after removing artifacts.
low-frequency (LF) band: an HRV frequency range of 0.04-0.15 Hz that may represent the influence of PNS and baroreflex activity when breathing or contracting muscles between 4.5-6.5 times a minute.
neurovisceral integration model: Thayer and Lane's theoretical framework describing the role of the central autonomic network (CAN) in regulating autonomic, cognitive, and emotional processes. It emphasizes the prefrontal cortex's top-down control over heart rate variability (HRV) via the vagus nerve, linking HRV to self-regulation and mental health.
norepinephrine (NE): an adrenal medullary hormone that initiates cardiac muscle
contraction when it binds to β1 receptors.
nucleus ambiguus system: the nucleus dorsal to the inferior olivary nucleus of the
upper medulla that gives rise to vagus nerve motor fibers.
peak frequency: the HRV frequency with the greatest power.
resonance: an amplification process in which an external force causes a closed-loop (negative feedback) system to oscillate with greater amplitude at its inherent resonance frequency (RF).
resonance frequency:
the frequency at which a system, like the cardiovascular system, can be activated or stimulated.
respiratory sinus arrhythmia (RSA):
the respiration-driven heart rhythm that contributes to the high frequency (HF) component of heart rate variability.
Inhalation inhibits vagal nerve slowing of the heart (increasing HR), while exhalation restores vagal slowing
(decreasing HR).
resting baseline: breathing at typical rates without pacing or feedback.
RMSSD: the square root of the mean squared difference of adjacent NN intervals in milliseconds.
SD1: the standard deviation of the distance of each point from the y = x-axis that measures short-term HRV.
SD2: the standard deviation of each point from the y = x + average RR interval that measures short- and long-term HRV.
SDNN: the standard deviation of the normal (NN) sinus-initiated IBI measured in milliseconds.
slow-paced breathing (SPB): low-and-slow breathing at ~ 6 bpm for adults with longer exhalation than inhalation.
slow-paced contraction (SPC): wrist-core-ankle contraction with legs supported and crossed at rates of ~1 or ~ 6 cpm.
spectral analysis: the division of heart rate variability into its component rhythms
that operate within different frequency bands.
sympathetically-mediated HRV (smHRV):spectral analysis: HRV components influenced by the sympathetic nervous system, typically assessed through measures such as low-frequency (LF) power in HRV analysis. However, the interpretation of LF power as a direct marker of sympathetic activity remains debated.
time-domain measures of HRV: indices like SDNN that quantify the total amount of heart rate variability.
triangular index (TI): a geometric measure based on 24-hour recordings, which calculates the integral of the RR interval histogram's density divided by its height.
triangular interpolation of the NN interval histogram (TINN): the baseline width of a histogram displaying NN intervals.
ultra-low-frequency (ULF) band: an ECG frequency range below 0.003 Hz. Very slow
biological processes that include circadian rhythms, core body temperature, metabolism, and the renin-angiotensin
system, and possibly the PNS and SNS, generate ULF activity.
vagal tank theory: Laborde and colleagues view cardiac vagal control as a dynamic resource for self-regulation, comprising resting vagal tone, reactivity to stress, and recovery. A higher vagal tank supports stress resilience, cognitive flexibility, and emotional regulation, while depletion leads to dysregulation and health risks.
vagally-mediated HRV (vmHRV): the high-frequency component of HRV, controlled by the parasympathetic nervous system via the vagus nerve. Indexed by the RMSSD and LF power during normal breathing, vmHRV serves as a biomarker of autonomic flexibility, with higher vmHRV indicating better cognitive control, emotional regulation, and stress resilience, while lower vmHRV is associated with poor health outcomes.
vagus nerve: the parasympathetic vagus (X) nerve decreases the rate of spontaneous
depolarization in the SA and AV nodes and slows HR. Heart rate increases often reflect reduced vagal
inhibition.
vascular tone (VT) baroreflex: the closed-loop encompassing the cardiovascular control center, vascular tone control system, and blood pressure control system.
very-low-frequency (VLF): an ECG frequency range of 0.003-.04 Hz that may represent
temperature regulation, plasma renin fluctuations, endothelial, physical activity influences, possible intrinsic cardiac nervous system, and PNS contributions.
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Assignment
Now that you have completed this module, monitor your HR as you inhale and exhale to observe your own RSA. What
is the average difference between your fastest and slowest HRs across several breathing cycles? How has this
unit changed how you might explain HRV and its potential benefits to a client.
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